Abstract

Considering that, for 99.9% of human history, physical activity was a key component of everyday human life, our ‘evolution’ into a sedentary species is all the more remarkable. In his seminal 1998 paper, Rowland clearly outlined the biological need of our bodies for physical activity, with candidate genes now being identified that might contribute to a physical activity (and inactivity) phenotype. However, much research has gone into psychosocial and environmental influences on physical activities over and above biological ones, and rightly so. Complex societal pathways exist to explain why one particular person—or indeed group of people—might be less active than another. Sallis and Owen outlined an ecological perspective, which postulated that human behaviour results from an interaction of individual (self-efficacy), social (social support) and environmental (eg, physical barriers to walking, access to public open space) factors.3 Their behavioural epidemiological framework is a tool which health policy makers can potentially use to translate into policy research findings that demonstrate the link between today's human behaviours and tomorrow's disease patterns.

It is clear that physical inactivity increases the risk of chronic disease and decreases life expectancy. Cardiovascular disease, thromboembolic stroke, hypertension, type 2 diabetes mellitus, osteoporosis, obesity, colon cancer, breast cancer, anxiety and depression have all been linked with physical inactivity.4 If—as in most chronic disease causation—a multi-factorial process exists to explain disease onset, what might be the relative role of physical inactivity in explaining disparate burdens of disease in differing populations? With a risk factor such as physical inactivity so intimately determined by broader social influences and physical facilities/surroundings, might this represent an opportunity for a broad-brush public health intervention to improve the health of a less healthy population?